A body of evidence suggests that disordered adrenal biosynthesis and production of known or unknown mineralocorticoids by the adrenal cortex is implicated in the pathogenesis of the hypertension of some patients, notably those with low plasma renin activities. I propose to evaluate adrenal function using two techniques, multiple plasma steroid responses to small graded ACTH infusions and to a small standard quantity of the 11-Beta-hydroxylase inhibitor metyrapone, in patients with low-renin essential hypertension and in comparison groups with normal renin hypertension and in normal controls. I then plan to treat all hypertensive patients for 12 weeks with low dose dexamethasone to achieve adrenal suppression using a double-blinded placebo controlled cross-over protocol in order to evaluate the effect of arrest of ACTH-dependent steroidogenesis upon each form of hypertension, and to correlate such responses with antecedent adrenal function. In a separate study, I plan to evaluate using multiple plasma steroid responses to ACTH, angiotensin II and potassium adrenal steroid biosynthesis in patients with the syndrome of hyporeninemic hypoaldosteronism and in a comparison group of patients known to be at risk for this syndrome, those with long-standing diabetes mellitus. To test the hypothesis that chronic renin deficiency is the cause of the described abnormalities of mineralocorticoid biosynthesis in this syndrome, I shall assess adrenal function both before and after chronic renin stimulation by oral furosemide. I hope to both clarify the mechanisms implicated in hyporeninemic hypoaldosteronism and evaluate a form of therapy alternative to pharmacologic doses of mineralocorticoids.